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首页> 外文期刊>Canadian Journal of Physiology and Pharmacology >Role of large-conductance Ca(2)(+)-activated K(+) channels in adenosine A receptor-mediated pharmacological postconditioning in H9c2 cells.
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Role of large-conductance Ca(2)(+)-activated K(+) channels in adenosine A receptor-mediated pharmacological postconditioning in H9c2 cells.

机译：大电导Ca（2）（+）激活K（+）通道在H9c2细胞中腺苷A受体介导的药理后处理中的作用。

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Ischaemic postconditioning is a phenomenon whereby short periods of ischaemia applied during the start of reperfusion protect the myocardium from the damaging consequences of reperfusion. As such, pharmacological-induced postconditioning represents an attractive therapeutic strategy for reducing reperfusion injury during cardiac surgery and following myocardial infarction. The primary aim of this study was to determine the role of large-conductance Ca(2)(+)-activated potassium channels (BK(Ca) channels) in adenosine A receptor-induced pharmacological postconditioning in the rat embryonic cardiomyoblast-derived cell line H9c2. H9c2 cells were exposed to 6 h hypoxia (0.5% O) followed by 18 h reoxygenation (H/R) after which cell viability was assessed by monitoring lactate dehydrogenase (LDH) release and caspase-3 activation. The adenosine A receptor agonist N-cyclopentyladenosine (CPA; 100 nmol/L) or the BK(Ca) channel opener NS1619 (10 micromol/L) were added for 30 min at the start of reoxygenation following 6 h hypoxic exposure. Where appropriate, cells were treated (15 min) before pharmacological postconditioning with the BK(Ca) channel blockers paxilline (1 micromol/L) or iberiotoxin (100 nmol/L). Pharmacological postconditioning with CPA or NS1619 significantly reduced H/R-induced LDH release. Treatment with paxilline or iberiotoxin attenuated adenosine A receptor and NS1619-induced pharmacological postconditioning. These results have shown for the first time that BK(Ca) channels are involved in adenosine A receptor-induced pharmacological postconditioning in a cell model system.
机译：缺血后处理是一种现象，在再灌注开始时施加短暂的局部缺血可以保护心肌免受再灌注造成的破坏性后果。这样，药理学诱导的后处理代表了一种有吸引力的治疗策略，用于减少心脏手术期间和心肌梗塞后的再灌注损伤。这项研究的主要目的是确定大电导Ca（2）（+）激活的钾通道（BK（Ca）通道）在大鼠胚胎心肌成纤维细胞衍生的腺苷A受体诱导的药理后处理中的作用H9c2。将H9c2细胞暴露于6 h缺氧（0.5％O），然后进行18 h复氧（H / R），然后通过监测乳酸脱氢酶（LDH）释放和caspase-3活化来评估细胞活力。缺氧暴露6小时后，在重新供氧30分钟后，添加腺苷A受体激动剂N-环戊基腺苷（CPA; 100 nmol / L）或BK（Ca）通道开放剂NS1619（10 micromol / L）。在适当的情况下，在药理学后处理之前，用BK（Ca）通道阻滞剂Paxilline（1 micromol / L）或iberiotoxin（100 nmol / L）处理细胞（15分钟）。用CPA或NS1619进行药理学后处理可显着降低H / R诱导的LDH释放。用paxilline或iberiotoxin减毒的腺苷A受体和NS1619诱导的药理后处理。这些结果首次表明BK（Ca）通道参与细胞模型系统中腺苷A受体诱导的药理后处理。

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